Evidence map›Paper›PMID 34350119›Full record

SynthesisFrontiers in oncology2021

Can Targeting Hypoxia-Mediated Acidification of the Bone Marrow Microenvironment Kill Myeloma Tumor Cells?

Gilberto Gastelum, Mysore Veena, Kylee Lyons, Christopher Lamb, Nicole Jacobs, Alexandra Yamada, Alisher Baibussinov, Martin Sarafyan, Rebeka Shamis, Jeffry Kraut and 1 more

Open access · goldAbstract readSystematic Review
PubMed Full text at PMC Publisher
In one paragraph

Synthesis in Frontiers in oncology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Autophagy-related mechanisms for treatment of multiple myeloma.Cancer drug resistance (Alhambra, Calif.) · 2023
    Review
  8. Review
  9. Review
  10. Article
  11. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Gilberto GastelumDepartment of Hematology/Oncology, University of California, Los Angeles, Los Angeles, CA, United States.
Mysore VeenaDepartment of Hematology/Oncology, University of California, Los Angeles, Los Angeles, CA, United States.
Kylee LyonsDepartment of Hematology/Oncology, University of California, Los Angeles, Los Angeles, CA, United States.
Christopher LambDepartment of Hematology/Oncology, University of California, Los Angeles, Los Angeles, CA, United States.
Nicole JacobsDepartment of Hematology/Oncology, University of California, Los Angeles, Los Angeles, CA, United States.
Alexandra YamadaDepartment of Hematology/Oncology, University of California, Los Angeles, Los Angeles, CA, United States.
Alisher BaibussinovDepartment of Hematology/Oncology, University of California, Los Angeles, Los Angeles, CA, United States.
Martin SarafyanDepartment of Hematology/Oncology, University of California, Los Angeles, Los Angeles, CA, United States.
Rebeka ShamisDepartment of Research, Greater Los Angeles Veterans Administration Healthcare System, Los Angeles, CA, United States.
Jeffry KrautDepartment of Hematology/Oncology, University of California, Los Angeles, Los Angeles, CA, United States.
Patrick FrostDepartment of Hematology/Oncology, University of California, Los Angeles, Los Angeles, CA, United States.
University of California, Los Angeles · USVA Greater Los Angeles Healthcare System · US

Funding

BLRD VA I01 BX004280
6 · The paper itself

Abstract

Multiple myeloma (MM) is an incurable cancer arising from malignant plasma cells that engraft in the bone marrow (BM). The physiology of these cancer cells within the BM microenvironment (TME) plays a critical role in MM development. These processes may be similar to what has been observed in the TME of other (non-hematological) solid tumors. It has been long reported that within the BM, vascular endothelial growth factor (VEGF), increased angiogenesis and microvessel density, and activation of hypoxia-induced transcription factors (HIF) are correlated with MM progression but despite a great deal of effort and some modest preclinical success the overall clinical efficacy of using anti-angiogenic and hypoxia-targeting strategies, has been limited. This review will explore the hypothesis that the TME of MM engrafted in the BM is distinctly different from non-hematological-derived solid tumors calling into question how effective these strategies may be against MM. We further identify other hypoxia-mediated effectors, such as hypoxia-mediated acidification of the TME, oxygen-dependent metabolic changes, and the generation of reactive oxygen species (ROS), that may prove to be more effective targets against MM.

Indexed as

acid base regulationbone marrow microenvironmenthypoxia and apoptosismultiple myelomapH balance

Identifiers

PMID34350119
PMCPMC8327776
OpenAlexW3185901606

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.